Bradykinin in reflex cardiovascular responses to static muscular contraction

1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Carboxypeptidase B ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Life Events, Cardiovascular Reactivity, and Risk Behavior in Adolescent Boys

PEDIATRICS ◽  
1995 ◽  
Vol 96 (6) ◽  
pp. 1101-1105
Author(s):  
Sai-Woon Liang ◽  
John M. Jemerin ◽  
Jeanne M. Tschann ◽  
Charles E. Irwin ◽  
Diane W. Wara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Risk Behavior ◽  
Arterial Blood Pressure ◽  
Life Events ◽  
Cardiovascular Reactivity ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Adolescent Boys ◽  
Positive Life Events ◽  
Arterial Blood

Background. Risk behavior contributes to injuries, one of the most important sources of morbidity and mortality in adolescents. Although research has shown that environmental stress makes adolescents more likely to engage in risk behavior and to sustain injuries, the magnitude of these associations has been small. Little is known about the role of individual differences in psychobiologic reactivity to stress in moderating the impact of stressful events. In this study, we examined associations among environmental stressors, cardiovascular reactivity to stress, and the level of risk behavior in adolescent boys. Methods. Twenty-four 14- to 16-year-old boys underwent a laboratory protocol designed to measure responses to psychologically and physically stressful tasks. Changes in heart rate and mean arterial blood pressure were measured serially at standard points in the protocol, and levels of positive and negative life events and recent risk behavior were measured using self-report questionnaires. Results. Neither life events nor cardiovascular reactivity were independently associated with risk behavior. Positive life events and mean arterial blood pressure reactivity significantly interacted, however, in predicting risk behavior (R2 increment = .25). Boys with high reactivity who reported numerous positive life events engaged in markedly less risk behavior than their peers. Conclusion. We conclude that adolescents with exaggerated cardiovascular responses to laboratory stressors are associated with less risk behavior in a setting of positive life circumstances. This result suggests that reactivity may exert protective, rather than harmful, influences in some environments.

Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

Cardiovascular response to arousal from sleep under controlled conditions of central and peripheral chemoreceptor stimulation in humans

2004 ◽  
Vol 96 (3) ◽  
pp. 865-870 ◽  
Author(s):  
Denise M. O'Driscoll ◽  
Guy E. Meadows ◽  
Douglas R. Corfield ◽  
Anita K. Simonds ◽  
Mary J. Morrell
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Peripheral Chemoreceptor ◽  
Healthy Men ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia

The cardiovascular response to an arousal occurring at the termination of an obstructive apnea is almost double that to a spontaneous arousal. We investigated the hypothesis that central plus peripheral chemoreceptor stimulation, induced by hypercapnic hypoxia (HH), augments the cardiovascular response to arousal from sleep. Auditory-induced arousals during normoxia and HH (>10-s duration) were analyzed in 13 healthy men [age 24 ± 1 (SE) yr]. Subjects breathed on a respiratory circuit that held arterial blood gases constant, despite the increased ventilation associated with arousal. Arousals were associated with a significant increase in mean arterial blood pressure at 5 s ( P < 0.001) and with a significant decrease in the R-R interval at 3 s ( P < 0.001); however, the magnitude of the changes was not significantly different during normoxia compared with HH (mean arterial blood pressure: normoxia, 91 ± 4 to 106 ± 4 mmHg; HH, 91 ± 4 to 109 ± 5 mmHg; P = 0.32; R-R interval: normoxia, 1.12 ± 0.04 to 1.02 ± 0.05 s; HH, 1.09 ± 0.05 to 0.92 ± 0.04 s; P = 0.78). Mean ventilation increased significantly at the second breath postarousal for both conditions ( P < 0.001), but the increase was not significantly different between the two conditions (normoxia, 5.35 ± 0.40 to 9.57 ± 1.69 l/min; HH, 8.57 ± 0.63 to 11.98 ± 0.70 l/min; P = 0.71). We conclude that combined central and peripheral chemoreceptor stimulation with the use of HH does not interact with the autonomic outflow associated with arousal from sleep to augment the cardiovascular response.

Abstract 446: Rostral Ventrolateral Lateral Medulla Mediates the Sympathetic and Cardiovascular Response to Increased Cerebrospinal Fluid Sodium Concentration

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sean D Stocker
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Lateral Ventricle ◽  
Cardiovascular Response ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Nerve Recordings

Compelling evidence indicates increased cererbrospinal fluid (CSF) sodium elevates sympathetic nerve activity (SNA) and arterial blood pressure (ABP) in salt-sensitive hypertension. RVLM neurons project to the spinal cord and regulate SNA and ABP under a number of physiological challenges and pathophysiological states. Therefore, we hypothesized that RVLM neurons mediate the sympathoexcitatory response to increased CSF sodium. Inactin-anesthetized, male Sprague-Dawley rats (n=5/group) were prepared for sympathetic nerve recordings and a lateral ventricle brain cannula. Infusion of 1M NaCl (5 μL/10 min) to increase CSF sodium concentrations by 5mM produced a significant (P’s<0.05, n=6) increase in lumbar SNA (Δ: 115±3%), adrenal SNA (Δ: 122±3%), and mean arterial blood pressure (Δ: 8±1 mmHg). The infusion did not affect splanchnic SNA (Δ: 102±4%) but decreased renal SNA (Δ: 91±2%). Inhibition of the RVLM with bilateral injection of the GABA agonist muscimol (2.5mM per 50 nL per side) significantly (P’s<0.05; n=5) attenuated the increased lumbar SNA (Δ:101±2%), adrenal SNA (Δ:105±2%), and mean arterial blood pressure (Δ: 1±1mmHg, P’s<0.05; n=6). Blockade of ionotropic glutamate receptors in the RVLM with bilateral injection of kynurenic acid (30mM per 50 nL per side) also significantly (P’s<0.05; n=5) attenuated the increase in lumbar SNA (Δ: 101±3%), adrenal SNA (Δ: 110±3%) and mean ABP (Δ: 1±2 mmHg) to lateral ventricle infusion of 1M NaCl (5uL/10 min). In a final set of experiments, in vivo single-unit recordings demonstrate that ventricular infusion of 1M NaCl (5uL per 10 min) increased discharge in 60% (6/10) of spinally-projecting, barosensitive RVLM neurons (2.1±0.4 to 5.8±0.2 Hz, P<0.05). Infusion of artificial CSF did not affect any variable. These findings suggest increased CSF sodium activates a glutamatergic pathway to RVLM neurons to elevate SNA and ABP.

scholarly journals Role of oral gabapentin in attenuating cardiovascular response to laryngoscopy and tracheal intubation.

2020 ◽  
Vol 27 (07) ◽  
pp. 1470-1475
Author(s):  
Mohsin Riaz Askri ◽  
Shumyala Maqbool ◽  
Kausar Abbas Shah ◽  
Shahbaz Ahmad
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tracheal Intubation ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Arterial Blood ◽  
Group I ◽  
Group Ii

Objectives: To determine the role of 800 mg oral gabapentin in attenuating cardiovascular response to laryngoscopy and tracheal intubation. Study Design: Double Blind Randomized Control Trial. Setting: Independent University Hospital/Independent Medical College, Faisalabad, Pakistan. Period: Six months from January1st 2019 to June 30th 2019. Material & Methods: This study included 60 patients which were divided into two equal groups. 800 mg oral gabapentin was given to group I while capsule placebo was administrated to group II patients in pre-operative area one hour prior to surgery. Heart rate, systolic, diastolic and mean arterial blood pressure were taken after induction of anesthesia at base line and then 1,2,3,4,5,10 and 15 minutes after endotracheal intubation. SPSS version 11 was used to analyze the data. Heart rate systolic, diastolic and mean arterial blood pressure were dependent variables while placebo and gabapentin were independent variables. Results: Out of total 60 patients there were 36 (60 %) males and 24 (40 %) females. In group I mean age was 37.1 while in group II it was 36.3. As compare to group II there was decreased cardiovascular response in group I. There was a significant decrease in systolic blood pressure at 1,2 and 10 minutes; diastolic blood pressure at 3 minutes; heart rate at 10 and 15 minutes and mean arterial blood pressure at 3 minutes after induction in group I. Conclusion: Cardiovascular response to laryngoscopy and intubation is significantly reduced with oral gabapentin.

scholarly journals Alterations in the Baroreceptor-Heart Rate Reflex in Conscious Inbred Polydipsic (STR/N) Mice

2015 ◽  
pp. 173-182
Author(s):  
C. P. CHU ◽  
B. R. CUI ◽  
H. KANNAN ◽  
D. L. QIU
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Baroreceptor Reflex ◽  
Central Administration ◽  
Icr Mice ◽  
Arterial Blood ◽  
And Control

STR/N is an inbred strain of mice which is known to exhibit extreme polydipsia and polyuria. We previously found central administration of angiotensin II enhanced cardiovascular responses in STR/N mice than normal mice, suggesting that STR/N mice might exhibit different cardiovascular responses. Therefore, in this study, we investigated daily mean arterial blood pressure and heart rate, and changes in the baroreceptor-heart rate reflex in conscious STR/N mice and control (ICR) mice. We found that variability in daily mean arterial blood pressure and heart rate was significantly larger in STR/N mice than in ICR mice (p<0.05). There was a stronger response to phenylephrine (PE) in STR/N mice than in ICR mice. For baroreceptor reflex sensitivity, in the rapid response period, the slopes of PE and sodium nitroprusside (SNP) were more negative in STR/N mice than in ICR mice. In the later period, the slopes of PE and SNP were negatively correlated between heart rate and blood pressure in ICR mice, but their slopes were positively correlated in STR/N mice. These results indicated that STR/N mice exhibited the different cardiovascular responses than ICR mice, suggesting that the dysfunction of baroreceptor reflex happened in conscious STR/N mice.

Muscle mechanosensitive receptors close to the myotendinous junction of the Achilles tendon elicit a pressor reflex

2007 ◽  
Vol 102 (6) ◽  
pp. 2112-2120 ◽  
Author(s):  
Tomoko Nakamoto ◽  
Kanji Matsukawa
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Achilles Tendon ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Myotendinous Junction ◽  
Arterial Blood ◽  
Pressor Reflex ◽  
Passive Stretch

Feedback regulation by activation of mechanosensitive afferents in the exercising muscle causes the cardiovascular and sympathetic nerve responses, which follow tension development and are almost identical between static contraction and passive stretch. The precise location of the mechanoreceptors contributing to the exercise pressor reflex, however, remained unknown. To test the hypothesis that the mechanoreceptors will be located around the myotendinous junction to monitor a change in muscle tension than a change in muscle length, we examined the reflex cardiovascular responses to passive stretch of the triceps surae muscle in anesthetized rats with three interventions; systemic injection of gadolinium, cutting the Achilles tendon, and local injection of lidocaine into the myotendinous junction. Gadolinium (42 μmol/kg iv) blunted the increases in heart rate and mean arterial blood pressure during passive stretch by 36 and 22–26%, respectively, suggesting that the reflex cardiovascular responses were evoked by stimulation of muscle mechanosensitive receptors. The cardiovascular responses to passive stretch were not different between the cut Achilles tendon and the intact tendon in the same rats, suggesting that any mechanoreceptors, terminated in the more distal part of the tendon, did not contribute to the reflex cardiovascular responses. Lidocaine (volume, 0.04–0.1 ml) injected into the myotendinous junction blunted the stretch-induced increases in heart rate and mean arterial blood pressure by 37–49 and 27–34%, respectively. We conclude that the muscle mechanosensitive receptors evoking the reflex cardiovascular responses at least partly locate at or close to the myotendinous junction of the Achilles tendon.

Changes in cardiac output and vascular resistance during behavioral stress in the rat

1986 ◽  
Vol 251 (1) ◽  
pp. R82-R90 ◽  
Author(s):  
J. W. Hubbard ◽  
R. H. Cox ◽  
B. J. Sanders ◽  
J. E. Lawler
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Plasma Norepinephrine ◽  
Wky Rats ◽  
Arterial Blood ◽  
Behavioral Stress

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.

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